Mechanism of anticancer agents and carcinogenesis in glioblastoma detected with markers for DNA damege

γ - h2ax是DNA双链断裂的有用标记物。目前的研究表明，抗胶质瘤药物的作用依赖于细胞系，细胞周期阻滞和/或衰老在其作用中起主要作用。胶质瘤的恶性进展可能与抑制细胞对DNA损伤的反应有关，因为胶质瘤病理标本中H2AX阳性随着胶质瘤级别的增加而增加。在胶质瘤中，许多具有明显多形性的细胞核显示出严重的DNA损伤和细胞增殖标记物的阳性。这些结果表明，严重的DNA损伤诱导核多形性，而核多形性不一定是恶性肿瘤的直接证据。

gamma-H2AX is a useful marker for DNA double strand breaks. Present study revealed that effects of anti-cancer drugs in glioma depend on cell lines, and cell cycle arrest and/or senescence play major roles in the effects. Progression of malignancy in glioma might be associated with inhibition of cell responses for DNA damages, since pathological specimens of glioma showed increasing positivity for H2AX as the grade of the glioma increased. In glioma, lots of nuclei with significant pleomorphism demonstrated both severe DNA damage and positivity for a cell-prolirerating marker. These results implies severe DNA damage induces nuclear pleomorphism and nuclear pleomorphism is not necessarily a direct evidence for malignancy.